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Published on: November 9, 2019
Dexras1 potentiates photic and suppresses nonphotic responses of the circadian clock
Hai-Ying M Cheng1, Karl Obrietan, Sean W Cain
1Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr. Bohr Gasse 3-5, A-1030 Vienna. hymcheng@yahoo.ca
Abstract:
Circadian rhythms of physiology and behavior are generated by biological clocks that are synchronized to the cyclic environment by photic or nonphotic cues. The interactions and integration of various entrainment pathways to the clock are poorly understood. Here, we show that the Ras-like G protein Dexras1 is a critical modulator of the responsiveness of the master clock to photic and nonphotic inputs. Genetic deletion of Dexras1 reduces photic entrainment by eliminating a pertussis-sensitive circadian response to NMDA. Mechanistically, Dexras1 couples NMDA and light input to Gi/o and ERK activation. In addition, the mutation greatly potentiates nonphotic responses to neuropeptide Y and unmasks a nonphotic response to arousal. Thus, Dexras1 modulates the responses of the master clock to photic and nonphotic stimuli in opposite directions. These results identify a signaling molecule that serves as a differential modulator of the gated photic and nonphotic input pathways to the circadian timekeeping system.
Insights
The study identifies Dexras1 as a key protein regulating the body's internal clock. Dexras1 differentially controls how light and non-light cues synchronize circadian rhythms.
Area of Science:
- Chronobiology
- Molecular Biology
- Neuroscience
Background:
- Circadian rhythms govern physiological and behavioral cycles.
- Biological clocks synchronize to environmental cues (light/dark, etc.).
- Integration of entrainment pathways to the master clock remains unclear.
Purpose of the Study:
- Investigate the role of Dexras1 in modulating circadian clock responses.
- Elucidate Dexras1's function in integrating photic and nonphotic entrainment pathways.
Main Methods:
- Genetic deletion of Dexras1 in mice.
- Assessment of photic entrainment using NMDA stimulation.
- Evaluation of nonphotic entrainment using neuropeptide Y and arousal stimuli.
- Analysis of signaling pathways including Gi/o and ERK activation.
Main Results:
- Dexras1 deletion impairs photic entrainment by disrupting NMDA response.
- Dexras1 couples NMDA and light signals to Gi/o and ERK pathways.
- Mutation potentiates neuropeptide Y responses and unmasks arousal-induced nonphotic entrainment.
- Dexras1 acts as a differential modulator, opposing effects on photic and nonphotic inputs.
Conclusions:
- Dexras1 is a critical signaling molecule for circadian clock responsiveness.
- It differentially modulates photic and nonphotic entrainment pathways.
- Identifies Dexras1 as a key integrator of environmental cues for circadian timekeeping.
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